Aaron J. Marcus: in pursuit of perfection.

Dr. Aaron Jacob Marcus, Professor of Medicine at Weill Cornell Medical College and distinguished physician-scientist in hematology and vascular biology, passed away on May 6, 2015 (Figure 1). Aaron Marcus was born in 1925 in Brooklyn, New York, where he attended Boys High School (1939–1943). His formal education at the University of Virginia (1943–1944; 1946–1948) was interrupted by his service as a pharmacist’s mate in the United States Navy during World War II (1944–1946). In 1953, he received his MD degree from New York Medical College, where he was elected to Alpha Omega Alpha. Following a rotating internship at Jewish Hospital of Brooklyn (1953–1954), he completed residency training in internal medicine at Montefiore Hospital (1954–1956) and served there as a fellow in hematology under Theodore H. Spaet (1956–1958). His subsequent career spanned more than fifty years. He was an attending physician and Chief of Hematology-Oncology at the New York Veterans Administration (VA) Harbor Healthcare System (1958–2015) and an attending physician at New York– Presbyterian Hospital (1968–2015). He was Professor of Medicine (1973–2015) as well as Professor of Medicine in Pathology and Laboratory Medicine (1990–2015) at Weill Cornell Medical College. As a friend and colleague for many years at Weill Cornell Medical College, I was fortunate to know and admire both his record of scientific excellence and his generous nature. Dr. Marcus’s contributions to hematology are legendary. In his initial research papers, he carried out the first comprehensive isolation of platelet lipids and demonstrated that phosphatidylserine was unique in its ability to replace platelets in thromboplastin generation and prothrombin consumption tests (1, 2). These findings led to the development of the partial thromboplastin time used in clinical coagulation studies today. Based on his pioneering platelet fractionation studies, he concluded that platelet membranes furnished the catalytic surface for formation of the prothrombin activator complex (3). He reported the production of platelet superoxide, which, he speculated, might shorten the life span of platelets in vitro or modulate their behavior in vivo (4). He demonstrated that the acetyl group of acetylsalicylic acid (aspirin) bound irreversibly to cyclooxygenase, thus inhibiting the production of platelet-specific eicosanoids